John Leonora

Relationship of Fluid Transport Through the Dentin to the Incidence of Dental Caries

The rate of fluid movement in the teeth of 28-day-old rats is inversely related to the incidence of dental caries after 13 weeks of the same diets. The early hypomineralization found in the dentin at 28 days is a result of altered metabolism imposed by a reduced rate of fluid transport in the rats fed a cariogenic diet.

The Effect of Desalivation Upon Pulpal Function and Dental Caries in Rats

The role of pulp and saliva in caries susceptibility and resistance was evaluated using a combination of endodontic treatment and desalivation. Evidence was presented that the pulp plays a major role in caries susceptibility. It is suggested that pulpal function is modified by hormonal factor(s) originating from salivary glands. In the rat, saliva appears to play a minor role in resistance to caries.

The effect of dietary factors on intradentinal dye penetration in the rat

Fluorescent dye injected systemically into rats penetrated the dentinal tubules of molar teeth in a dynamic fashion. The presence of dye was established using histological and fluorescence microscopy techniques. The rate of intradentinal dye penetration was dependent on dietary factors: it was high in rats chronically fed Purina rat chow and low in rats fed a cariogenic, high-sucrose diet. In addition, parotidectomized rats showed low levels of intradentinal dye penetration, even though they were maintained on Purina chow. One and 2 ml of plasma from Purina-fed rats were effective in stimulating the dye penetration in intact and parotidectomized rats, whereas 2 and 4 ml of plasma from rats fed a high-sucrose diet were ineffective when infused in either intact or parotidectomized animals. The results suggest that rats fed Purina chow have a significantly higher titre of a circulating, dye penetration stimulating factor than animals fed a high sucrose diet. This circulating factor could be the equivalent of the parotid hormone isolated from porcine tissue. It is suggested that dietary factors may affect secretion of a parotid hormone and thereby regulate the rate of dentinal fluid movement. There is therefore the prospect of a functional relationship between diet, the regulation of dentinal fluid flow by an endocrine system and dental health.

Effect of Infusing Selected Chemical Compounds on Dentinal Fluid Movement in the Rat

Intra-arterial infusion of carbamyl phosphate or of carbamyl-DL-aspartic acid into rats on a cariogenic diet greatly stimulated the movement of fluid through the odontoblastic processes. The infusion of sodium cyanate also stimulated fluid movement. Guanidine HCl and L-asparagine were active at higher concentrations. Purifying the urea on a mixed-bed ion exchange resin virtually removed its stimulatory effect on dentinal fluid movement. The action of urea is apparently attributable to contamination with sodium cyanate.

Further evidence for a hypothalamus-parotid gland endocrine axis in the rat

The existence of a hypothalamus-parotid gland endocrine axis that stimulates intradentinal dye penetration (IDDP) in rat teeth was suggested in earlier studies and IDDP-stimulating factors were isolated or purified from porcine parotid glands and hypothalamic tissues, respectively. In the present study, infusion of carbamyl-DL-aspartic acid (CAA) into rats was used to demonstrate the role of the endogenous hormones of the hypothalamus-parotid gland endocrine axis in stimulating IDDP, as observed by fluorescence microscopy of longitudinal sections of molar teeth. Intra-arterial infusion of CAA into intact rats stimulated IDDP in a dose-related fashion (between 49-390 nmol/100 g body weight); however, infusion of 390 nmol into parotidectomized rats was ineffective. Infusion of plasma from CAA-treated rats was equally effective in stimulating IDDP in intact and in parotidectomized animals. In contrast, plasma obtained from parotidectomized, CAA-treated rats stimulated IDDP in intact recipient animals but not in parotidectomized ones. Moreover, plasma from adult rats treated with CAA after an electrolytic lesion of the hypothalamus, and infused back into young intact rats, was ineffective in stimulating IDDP. These results indicate that: (1) CAA requires the functional integrity of the parotid gland to express its IDDP-stimulating activity, (2) a hormonal factor is secreted by the parotids in response to CAA stimulation and is directly responsible for IDDP stimulation, (3) release of the endocrine parotid IDDP-stimulating factor after infusion of CAA involves a second endocrine factor that appears to originate from the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of Selected Dietary Additives on the Incidence of Dental Caries in the Rat

Weanling rats fed a cariogenic diet supplemented with carbamyl phosphate, in combination with egg shell meal and trace elements, showed a striking reduction in the incidence of caries. The cariostatic efficacy of carbamyl phosphate is significant because it stimulates fluid movement within odontoblasts via the hypothalamic-parotid gland endocrine axis.

Parotid Gland Function and Dentin Apposition in Rat Molars

Previous studies have clearly established the down-regulating effect of a sucrose-rich diet on primary dentinogenesis in rat molars. Earlier observation of the negative effect of a high-sucrose diet on a parotid function involved in the control of intradentinal solute movement led us to hypothesize that parotid gland function(s) may have a role in regulating dentinogenesis. Dentin apposition in 1st and 2nd molars of young rats was measured by planimetry in sagittal sections. The following experimental variables were tested: standard and high-sucrose diets, removal of the parotid or the submandibular/sublingual glands, and diets in powder or pellet form. Removal of the submandibular/sublingual glands and changes in diet consistency did not significantly affect dentin apposition. Dentin apposition was significantly depressed by the high-sucrose diet or following parotidectomy. A further decrease followed the combination of the two treatments. Parotid glands appeared to exert a positive effect on dentin apposition in rat molars.

Effect of dietary carbamyl phosphate on dentine apposition in rat molars.

In rats, sucrose increases dental caries and impairs odontoblastic function by reducing dentine apposition during primary dentinogenesis. A high-sucrose diet also affects negatively a pulp or dentine function that appears to regulate solute or fluid movement within rat dentinal tissue. In earlier work it was found that carbamyl phosphate could significantly reverse sucrose-induced cariogenesis and also stimulate sucrose-depressed movement of dentinal fluid through a mechanism involving parotid function(s). In the current study, the possibility that carbamyl phosphate could overcome the sucrose-induced reduction in dentine apposition was examined. Weanling rats were fed a high-sucrose diet supplemented or not with carbamyl phosphate for 5 weeks. Dentine apposition was measured planimetrically in sagittal sections of the molars. The effect of carbamyl phosphate was similarly tested in parotidectomized animals. Carbamyl phosphate significantly reduced the deleterious effect of sucrose on dentine apposition by 58% in the first molars. However, the reduction in dentine apposition that followed parotidectomy was not altered by carbamyl phosphate supplementation. The possibility that the beneficial effect of carbamyl phosphate on dentinogenesis involves a parotid function is entertained.

Stimulation of intradentinal dye penetration by feeding in the rat

Dentinal fluid movement, as measured by intradentinal dye penetration (IDDP), may be under the control of an endocrine system that includes the parotid glands. It was earlier demonstrated that parotid hormone stimulates IDDP when infused into rats, and in the pig the onset of feeding signals the release into the circulation of immunoreactive parotid hormone (iPH), the titre of which remains elevated for more than 1 h after feeding. As, for technical reasons, it is impossible to measure iPH and IDDP activity in the same animal, the hypothesis that feeding causes IDDP stimulation in the rat was now tested. Feeding rats for 15 min stimulated IDDP to a level significantly higher than when fasting (0.418 +/- 0.040 versus 0.106 +/- 0.022, p < 0.001). Within the experimental conditions, IDDP stimulation lasted longer than 15 min. Sialoadenectomy before the feeding experiment did not change the feeding-stimulated IDDP response unless the parotid glands were removed. In parotidectomized and totally sialoadenectomized rats fed for 15 min, the level of IDDP was not different from that of sham-operated fasting animals. It is postulated that, in addition to the existence of possible local regulatory factors in the pulp, dentinal permeation may be under a physiological control mechanism involving a parotid endocrine function. It is also suggested that a hormonally controlled mechanism of dentinal fluid movement may play a systemic, protective role against the bacterial acidogenic challenge to teeth.

Biological and chemical evidence for the existence of a porcine hypothalamic parotid hormone-releasing factor

Methodology has been developed to achieve partial purification of a parotid hormone-releasing peptide from porcine hypothalamus-thalamus tissue using an in vivo parotid hormone stimulation test in pigs and a dentinal fluid transport stimulation test in rats. The purification steps include: acetone-water extraction of the tissue at pH 5.2, ultrafiltration through Amicon PM10 membrane, size exclusion chromatography on Bio-Gel P2, and open-column reversed-phase chromatography on Lichroprep RP8. A 100-fold increase in specific activity was attained. Intravenous infusion of porcine hypothalamus-thalamus extract stimulates a dentinal fluid transport mechanism in teeth of intact anesthetized rats, and the release of plasma immunoreactive parotid hormone in conscious catheterized pigs. Parotidectomy in both species suppresses the response, suggesting that the expression of parotid hormone-releasing activity requires the integrity of a putative hypothalamus-parotid gland endocrine axis.